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AIR PARTICULATE POLLUTION EXPOSURE INDUCES SYSTEMIC OXIDATIVE STRESS IN HEALTHY MICE
Citation:
Roberts, E. S. AND K L. Dreher. AIR PARTICULATE POLLUTION EXPOSURE INDUCES SYSTEMIC OXIDATIVE STRESS IN HEALTHY MICE. Presented at Experimental Cell Biology (FASEB), Washington, DC, April 17-21, 2004.
Description:
Air particulate pollution exposure induces systemic oxidative stress in healthy mice
Elizabeth S Roberts1 and Kevin L Dreher2. 1 College or Veterinary Medicine, NC State University, Raleigh, NC , 2US Environmental Protection Agency, NHEERL, RTP, NC
Epidemiological studies indicate that exposure to air particulate pollution is associated with increased cardiopulmonary morbidity and mortality within susceptible sub-populations. Causal emission sources and biological mechanism(s) for these associations have yet to be identified. This study examines the ability of a specific air pollution particulate, residual oil fly ash (ROFA), to induce cardiopulmonary oxidative stress in heme oxygenase-1 (HO-1) luciferase transgenic reporter mice. Transgenic mice were exposed by aspiration to either saline or ROFA (50 ug/mouse). HO-1 induction in lung and heart tissue protein extracts was measured by luciferase chemiluminescence at 2h, 6h, 12h, and 24h post-exposure. Pulmonary HO-1 levels were increased at 2h (p < 0.01) post-exposure and remained elevated at 24h post-exposure. However, cardiac HO-1 levels gradually increased over time with significant sustained induction observed at 24h (p < 0.05) post-exposure. These results demonstrate the ability of air pollution particles to induce both local and systemic oxidative stress which in turn may result in acute organ injury as well as potentially contribute to disease processes that have oxidative stress as a common pathological etiology. (This abstract does not reflect EPA policy).